Currently, public pay more attention to the adverse effect of
organophosphate pesticides on human and animal health and on the environment in developing nations.
Vitamin E may protect the hepatocyte and increase the function of liver. The study was to investigate the effects of
phoxim-induced hepatotoxicity on Sprague Dawley (SD) rats and the protection of
vitamin E. SD rats received by gavage 180 mg kg-1 (per
body weight) of
phoxim, 200 mg kg-1 (per
body weight) of
vitamin E, and phoxim + vitamin E. The results showed that exposure to
phoxim elevated liver coefficient;
glutamyl transpeptidase (GGT),
aspartate aminotransferase,
alkaline phosphatase, total
bilirubin, total
bile acid, and
alanine aminotransferase in the serum; ROS in the liver; and the expression of p53, Bax,
CYP2E1, ROS,
caspase-9,
caspase-8, and
caspase-3, while
phoxim caused a reduction of total
protein,
albumin, and
cholinesterase in the serum;
acetylcholinesterase, total
antioxidant capacity,
glutathione peroxidase, and
glutathione in the liver; and the expression of Bcl-2.
Vitamin E modified the
phoxim-induced hepatotoxicity by reducing the GGT in the serum,
malondialdehyde in the liver, and the expression of
CYP2E1 significantly. There were no significant changes of
globulin in the serum, the activity of
catalase in the liver, as well as expression levels of Fas and Bad in the liver. Overall, subacute exposure to
phoxim induced hepatic injury, oxidative stress damage, and cell apoptosis.
Vitamin E modified
phoxim-induced hepatotoxicity slightly. And,
vitamin E minimized oxidative stress damage and ultrastructural changes in rat hepatocytes notably.